Experiments will be performed to determine the mechanistic basis of endotoxin-induced tumor regression. Additional syngeneic tumors will be examined to test the hypothesis that the only tumors that completely regress in response to parenteral injection of endotoxin are those that are immunogenic enough to evoke the generation of a state of concomitant antitumor immunity. Concomitant immunity will be investigated in terms of the properties of the sensitized T-cells that mediate it, and in terms of whether the antitumor action of endotoxin is based on its capacity to potentiate the production of tumor-sensitized T-cells. The substitution of an intratumor delayed-sensitivity response to C. parvum or tumor specific immunity, in making tumors susceptible to endotoxin therapy, will be studied in terms of the nonspecific effector mechanism that C. parvum causes to develop in the tumors.